Abstract

To examine the impact of p21-activated kinase 1 on the growth, migration, apoptosis and invasion of hepatocellular carcinoma cells and its related mechanism. Hep38 was selected and divided into blank group, transfection control group and transfection group. The blank group was not given any treatment, the transfection control group was transfected with universal nonsense sequence, and the transfection group was given p21-activated kinases 1 sequence. The proliferation ability of cell counting kit-8 cells was compared by cell proliferation assay at different points in time after transfection. The cell cycle and apoptosis rate were detected by flow cytometry, the ability of cell migration was detected by scratch test, the p21-activated kinases 1/extracellular signal-regulated kinase pathway- related protein expression was found using the Western blot method, and the invasiveness of the cells in each group was assessed using the Transwell invasion test. The ability of cell proliferation in the transfection group was reduced than the blank group and the transfection control group at each time point. The proportion of cells in G1 phase in transfection group was reduced than blank group and transfection control group, while the proportion of G2/M phase in transfection group was higher than blank group and transfection control group. The apoptosis rate in the transfection group was higher than the blank group and the transfection control group. After 72 h of transfection, the number of invasive cells in the transfection group was reduced than the blank group and the transfection control group. After 24 h and 48 h of transfection, the cell migration ability of the transfection group was reduced than that blank group and the transfection control group. The expression of phosphorylated-p21-activated kinases 1 and phosphorylated-extracellular signal-regulated kinase 1/2 protein in the transfection group was reduced than the blank group and the transfection control group. Silencing the expression of the p21-activated kinases 1 gene can hinder hepatoma cell motility and invasion, decrease hepatoma cell proliferation, and cause apoptosis by causing cell arrest in the G2 shock M phase. Its suppression of the expression of proteins connected to the p21-activated kinases 1/extracellular signal-regulated kinase pathway could be the mechanism.